Complement cascade in severe forms of COVID‐19: Recent advances in therapy

Benmansour, Nassima Chouaki; Carvelli, Julien; Vivier, Éric

doi:10.1002/eji.202048959

Cited by 60 publications

(56 citation statements)

References 39 publications

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“…6,[15][16][17][18][19] Limited preliminary reports suggested a potential benefit of C5 blockade in severe forms of COVID-19, 6,15 but 2 prospective studies did not show any clear benefit of C5 or C5a blockade in this setting. 20,21 However, the patients here had mild pulmonary COVID-19 manifestations and absent or moderate markers of systemic complement activation. These findings suggest that TMA in our patients resulted predominantly from intrarenal complement activation and ensuing EC damage, associated to a genetic dysregulation of the complement alternative pathway in at least 4 patients (ie, a clinical and genetic pattern of renal TMA similar to the one reported in complement-mediated aHUS).…”

mentioning

confidence: 69%

COVID-19 as a potential trigger of complement-mediated atypical HUS

El-Sissy

Saldman

Zanetta

et al. 2021

Blood

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confidence: 69%

COVID-19 as a potential trigger of complement-mediated atypical HUS

El-Sissy

Saldman

Zanetta

et al. 2021

Blood

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“…COVID-19 pathogenesis is characterized by an initial virus-induced injury and consequent multi-organ failure, coupled with an intense inflammatory reaction, EC injury, and a prothrombotic coagulopathy with thrombotic events. The progression from mild to severe COVID-19 is characterized by the transition from an epithelial to an endothelial disease ( 14 , 68 ). Indeed, ECs, playing a pivotal role in the regulation of immune response, initiation, and maintenance of inflammatory process ( 69 ), coagulation, and platelet function, are key players in various pathological manifestations associated with COVID-19 ( Figure 3 ) ( 70 , 71 ).…”

Section: Endotheliitis Complement System and Pathogenesis Of Covid-19mentioning

confidence: 99%

COVID-19, Pre-Eclampsia, and Complement System

et al. 2021

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COVID-19 is characterized by virus-induced injury leading to multi-organ failure, together with inflammatory reaction, endothelial cell (EC) injury, and prothrombotic coagulopathy with thrombotic events. Complement system (C) via its cross-talk with the contact and coagulation systems contributes significantly to the severity and pathological consequences due to SARS-CoV-2 infection. These immunopathological mechanisms overlap in COVID-19 and pre-eclampsia (PE). Thus, mothers contracting SARS-CoV-2 infection during pregnancy are more vulnerable to developing PE. SARS-CoV-2 infection of ECs, via its receptor ACE2 and co-receptor TMPRSS2, can provoke endothelial dysfunction and disruption of vascular integrity, causing hyperinflammation and hypercoagulability. This is aggravated by bradykinin increase due to inhibition of ACE2 activity by the virus. C is important for the progression of normal pregnancy, and its dysregulation can impact in the form of PE-like syndrome as a consequence of SARS-CoV-2 infection. Thus, there is also an overlap between treatment regimens of COVID-19 and PE. C inhibitors, especially those targeting C3 or MASP-2, are exciting options for treating COVID-19 and consequent PE. In this review, we examine the role of C, contact and coagulation systems as well as endothelial hyperactivation with respect to SARS-CoV-2 infection during pregnancy and likely development of PE.

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“…Moreover, severe conditions have revealed histological accumulation of C4, MAC (membrane attack complex) which is interconnected with conditions like endotheliitis and microthrombi [ 77 ]. Thus, complement cascade may lead to procoagulant conditions and microvascular damage in advanced COVID 29 cases [ 78 ].…”

Section: Immune Pathogenesis During Covid-19 Infectionmentioning

confidence: 99%

Molecular Insights into the Crosstalk Between Immune Inflammation Nexus and SARS-CoV-2 Virus

Bose

Sunita²,

Pattanayak

2021

Curr Microbiol

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COVID-19, a type of viral pneumonia caused by severe acute respiratory syndrome coronavirus 2 has challenged the world as global pandemic. It has marked the identification of third generation of extremely pathogenic zoonotic coronaviruses of twenty-first century posing threat to humans and mainly targeting the lower respiratory tract. In this review, we focused on not only the structure and virology of SARS-COV-2 but have discussed in detail the molecular immunopathogenesis of this novel virus highlighting its interaction with immune system and the role of compromised or dysregulated immune response towards disease severity. We attempted to correlate the crosstalk between unregulated inflammatory outcomes with disrupted host immunity which may play a potential role towards fatal acute respiratory distress syndrome that claims to be life-threatening in COVID-19. Exploration and investigation of molecular host-virus interactions will provide a better understanding on the mechanism of fatal COVID-19 infection and also enlighten the escape routes from the same. Supplementary Information The online version contains supplementary material available at 10.1007/s00284-021-02657-9.

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Complement cascade in severe forms of COVID‐19: Recent advances in therapy

Cited by 60 publications

References 39 publications

COVID-19 as a potential trigger of complement-mediated atypical HUS

COVID-19 as a potential trigger of complement-mediated atypical HUS

COVID-19, Pre-Eclampsia, and Complement System

Molecular Insights into the Crosstalk Between Immune Inflammation Nexus and SARS-CoV-2 Virus

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